Researchers managed to breed the defect out of epileptic mice by balancing "good" and "bad" genes - the researchers found genes without the defective version of ATP1A3
cancelled out genes with it during breeding.
By breeding these epileptic mice with mice that had an extra copy of a non-defective version of ATP1A3
gene, the research team noticed that their offspring were born without this debilitating condition.
Using AHCF funding, we studied the functional impact of patient-specific mutations in the ATP1A3
gene, and it became clear that an organized clinic for children with AHC would not only help optimize care for these patients, but also allow us to better refine our outstanding research questions.